Journal
JOURNAL OF IMMUNOLOGY
Volume 166, Issue 10, Pages 6007-6011Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.166.10.6007
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Funding
- NCI NIH HHS [CA38355, CA25803] Funding Source: Medline
- NIAID NIH HHS [AI21487] Funding Source: Medline
- NIA NIH HHS [AG01743] Funding Source: Medline
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Unlike naive T cells, memory phenotype (CD44(high)) T cells exhibit a high background rate of turnover in vivo. Previous studies showed that the turnover of memory phenotype CD8(+) (but not CD4(+)) cells in vivo can be considerably enhanced by products of infectious agents such as LPS. Such stimulation is TCR independent and hinges on the release of type I IFNs (IFN-I) which leads to the production of an effector cytokine, probably IL-15. In this study, we describe a second pathway of CD44(high) CD8(+) stimulation in vivo. This pathway is IFN-gamma rather than IFN-I dependent and is mediated by at least three cytokines, IL-12, IL-18, and IFN-gamma. As for IFN-I, these three cytokines are nonstimulatory for purified T cells and under in vivo conditions probably act via production of IL-15.
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